Browsing by Author "Duran, Gizem Ayna"

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Extraction and Characterization of Chitin and Chitosan from Shrimp Shell and Squid Pen Waste: Application in Biofilm Production
(Institute of Electrical and Electronics Engineers Inc., 2025) Geckin, Duygu; Krotau, Yaraslau; Duran, Gizem Ayna
Citation - WoS: 2
Citation - Scopus: 2
Identification of Potential Inhibitors for Drug Resistance in Acute Lymphoblastic Leukemia Through Differentially Expressed Gene Analysis and in Silico Screening
(Academic press inc elsevier science, 2024) Özay, Başak; Tükel, Ezgi Yağmur; Ayna Duran, Gizem; Kiraz, Yağmur; Duran, Gizem Ayna
Acute lymphoblastic leukemia (ALL) is a disease of lymphocyte origin predominantly diagnosed in children. While its 5-year survival rate is high, resistance to chemotherapy drugs is still an obstacle. Our aim is to determine differentially expressed genes (DEGs) related to Asparaginase, Daunorubicin, Prednisolone, and Vincristine resistance and identify potential inhibitors via docking. Three datasets were accessed from the Gene Expression Omnibus database; GSE635, GSE19143, and GSE22529. The microarray data waes analyzed using R4.2.0 and Bioconductor packages, and pathway and protein-protein interaction analysis were performed. We identified 1294 upregulated DEGs, with 12 genes consistently upregulated in all four resistant groups. KEGG analysis revealed an association with the PI3K-Akt pathway. Among DEGs, 33 hub genes including MDM2 and USP7 were pinpointed. Within common genes, CLDN9 and HS3ST3A1 were subjected to molecular docking against 3556 molecules. Following ADMET analysis, three drugs emerged as potential inhibitors: Flunarizine, Talniflumate, and Eltrombopag. Molecular dynamics analysis for HS3ST3A1 indicated all candidates had the potential to overcome drug resistance, Eltrombopag displaying particularly promising results. This study promotes a further understanding of drug resistance in ALL, introducing novel genes for consideration in diagnostic screening. It also presents potential inhibitor candidates to tackle drug resistance through repurposing.
LEP and FOXO1 Genes, as a Proposed Tumor Suppressor Autophagic Cell Death Related Genes, Can Be Targeted by Antidiabetic Therapy in Nondiabetic Breast Cancer Patients
(Springer, 2025) Duran, Gizem Ayna; Kiraz, Yagmur; Baykara, Deniz
Introduction Breast cancer can be treated effectively with personalized, gene-targeted therapies due to its molecular and genetic differences. Our study aims to identify breast cancer-specific tumor suppressor genes related to autophagic cell death and discover new drugs that target these mechanisms, even if they are not breast cancer-specific. Materials and methods Gene intensity values of 457 tumor and 19 healthy breast tissues were used to determine downregulated and upregulated genes related to autophagy and apoptosis using Bioconductor R program via LIMMA package. Then, genes affecting survival were identified by survival analysis via Kaplan-Meier Plotter tool. Furthermore, the signalling pathways associated with these genes and targeting candidate drug components were determined by gene enrichment analysis using "KEGG pathway option" and Drug MATADOR in "ShinyGo 0.82" web-tool, respectively. Results Breast cancer tumor tissues showed downregulation of genes related to autophagy and apoptosis (c19orf12, CRYAB, LEP, SRPX, SNCA, FOXO1) and upregulation of others (SLC7A5, ATP2A2, INHBA, ATP5IF1). Among these, SLC7A5, c19orf12, LEP, SPRX, SNCA, and FOXO1 affected patient survival and prognosis. The AMPK signaling pathway, targeting FOXO1 and LEP, was identified as key. Only the LEP gene was targeted by Metformin, Pioglitazone, Rosiglitazone, and Troglitazone. Conclusion In our study, survival associated LEP and FOXO1 genes were identified as candidate tumor suppressor genes associated with autophagic cell death in non-obese and non-diabetic breast cancer patients. Anti-diabetic drugs such as Metformin, Pioglitazone, Rosiglitazone, Troglitazone are proposed as candidate components in the treatment processes by targeting the LEP gene in nondiabetic breast cancer patients.